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<p>Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large amounts of subviral particles containing its surface antigen (HBsAg). T cell immunity is crucial for controlling and clearing HBV infection. However, the intercellular processes underlying HBsAg presentation to T cells are incompletely understood. Here, using preclinical mouse models, we show that, following HBsAg expression, the intrahepatic Batf3<sup>+</sup>XCR1<sup>+</sup>CCR7<sup>-</sup> conventional dendritic cell subset cDC1 presents HBsAg by MHC-I cross-dressing, driving CD8<sup>+</sup> T cell response. Meanwhile, upon HBsAg access to lymphoid tissues, B cells acquire HBsAg directly in the follicles of lymphoid tissues and initiate CD4<sup>+</sup> T cell responses sequentially in the follicular and interfollicular regions, guided by chemoattractant receptors CCR5 and EBI2, respectively. Finally, we identify ALCAM, LFA-1, and CD80 as key co-stimulatory signals essential for optimal T cell responses. Thus, these findings reveal the roadmap of non-canonical antigen presentation that drives T cell immunity against HBsAg, advancing novel therapeutic strategies for chronic HBV infection.</p>

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Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月17日

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  • Xiaofang Li,
  • Wenxuan Sun,
  • Xiaolan Xu,
  • Qirong Jiang,
  • Yuheng Shi,
  • Huixi Zhang,
  • Weien Yu,
  • Bisheng Shi,
  • Simin Wan,
  • Jiangxia Liu,
  • Wuhui Song,
  • Jiming Zhang,
  • Zhenghong Yuan,
  • Jianhua Li

摘要

Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large amounts of subviral particles containing its surface antigen (HBsAg). T cell immunity is crucial for controlling and clearing HBV infection. However, the intercellular processes underlying HBsAg presentation to T cells are incompletely understood. Here, using preclinical mouse models, we show that, following HBsAg expression, the intrahepatic Batf3+XCR1+CCR7- conventional dendritic cell subset cDC1 presents HBsAg by MHC-I cross-dressing, driving CD8+ T cell response. Meanwhile, upon HBsAg access to lymphoid tissues, B cells acquire HBsAg directly in the follicles of lymphoid tissues and initiate CD4+ T cell responses sequentially in the follicular and interfollicular regions, guided by chemoattractant receptors CCR5 and EBI2, respectively. Finally, we identify ALCAM, LFA-1, and CD80 as key co-stimulatory signals essential for optimal T cell responses. Thus, these findings reveal the roadmap of non-canonical antigen presentation that drives T cell immunity against HBsAg, advancing novel therapeutic strategies for chronic HBV infection.